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40 Cards in this Set
- Front
- Back
Electrical synapse occur at
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gap junctions for instance
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Type of synapses Chemical synapses
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Axo-axonic
Axo-dendritic Axo-somatic |
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Glia communicates
through |
gap junctions
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Neurotransmitter transport is bidirectional, but faster in the
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orthograde direction
(away from the cell body) |
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Actions of Neurotransmitters
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Rapid activation of ion channels
• Slow, sustained activation or inhibition of ion channels • Modulation of ion channels (2nd messengers) • Activation or inhibition of gene transcription • Modification of morphology or synapse (These are order from fastest to slowest) |
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What makes a nt? Not only the fact of being present in
the neuron..for instance glutamate and GABA are in neurons but also throughout the body..so how to prove that they are released on cue from neuron |
Dye,
antibody etc..but it is no easy to show that they are there..but it is easier to screen for enzymes that make the neurotransmitters, usually antibodies use to screen for these enzymes but there's also protein synthesis on dendrites..for what? Receptors. These can be detected by pet |
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Estrogen has estrogen membrane bound receptors
allowing rapid enter and action through |
a gprotein
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Endocannabanoids ( resemble marihuana receptors)
A knock out of cb1 receptor can't sense |
marihuana like
substance..mouse become more sensitive to pain |
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A knockout of FAAH which breaks anandamide the
mouse becomes more resistant to |
pain
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Endocannabanoids
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cb1
FAAH Rimonabant |
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Rimonabant is a drug that reduce appetite and
smoking..but many people became suicidal or depressed..so this led to the conclusion that perhaps |
our natural endocannabanoids have an influence on our
mood |
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90% of our neurotransmission via
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glutamate (
excitatory) and GABA (INHIBITORY) |
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Ach about 10%function can be inhibitory of excitatory
depending on |
the receptor that binds...ach is
concentrated on basal forebrain |
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Neroepinephrine is about 1% or less...this is located in
brain stem..related to |
attention, mood and reward
system. |
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Dopamine on caudate. Important for
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movement and
reward system |
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Serotonoin in brain stem..involved in
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mood and appetite
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circadian rhythm
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Melatonin
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Certain receptors of Adenosine involved in
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adenosine
involved in migration and growth of dendritic spines |
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Nitric oxide lots in cerebellum and hyppocampus and
Cortex and is |
diffusable which is not common
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There is coexistence of peptides and small NTS in a
neuron, they can be differentiated by |
the train of stimuli
for which they released..under slow stimulus only one NTS may be released after increasing the stimulus more than one type of NTS may be released |
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Glutamate synthesis
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Glutamate is released, glutamate is up taken up.
Glutamate is broken down into glutamine and then transported itno the glutamate containing cell. Glutamase acts on glutamine and glutamate is made again. Limiting factor is the uptake of glutamate which will determine its availability in the cleft as well as the amount that is in the terminal |
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GABA synthesis
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Glutamate is being taken up which is acted
on by glutamine synthetase and makes glutamine..which in turn is acted on glutamate decarboxylase go give GABA and then GABA is released from cell. It is interesting that GABA and glutamate which antagonize each other use the same building blocks..this is so because when one gets high in concentration the other one gets regulated |
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Ach comes through pyruvate system..ach is limited by
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the availability of choline which is low
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Ach synthesis
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There choline
receptors on the cholinergic neurons which bring choline into the neuron when ach is broken down which is the main source. Also there is dietary choline from phosphotyl choline (lecitine) |
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Alzheimer's patient
seemed to lack ach..so why not give a supplement? |
plement..this
wouldnt work because as concentration of acetylcholine in the cholinergic neuron becomes adequate it inhibits the choline transport. |
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is cathecholamine substrate depedent?
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NO. Tyrosine and
phenylalanine is substrate for Catecholamine |
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Dopamine synthesis
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transporter. Tyrosine hydroxylase gives
dihydroxyne phenylalanine or dopa and they are acted on dopadecarboxylase to give dopam |
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dopamine. If a neuron is
a dopanergic it won't have dopamine betahydroxylase because |
dopamine is converted to neuroepinephrine is
made. If it is an epinephrine containing cell is going to have phenyl ethylonamine and phenyl ethyl transferase which converts norepinephrine into epinephrine |
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In Catecholamine synthesis tyrosine is not limited but
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the Pterin cofactor is limiting
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limiting. Lots of Catecholamine is
gonna compete for |
compete for the Pterin cofactor site on tyrosine
hydroxylase and inhibits it...tyrosine hydroxylase is the enzyme limiting and all Catecholamine synthesis require tyrosine hyd |
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hydroxylase. As we get more Nerve
activity more cyclic camp and calcium which phosphorylase tyrosine hydroxylase to inhibit the enzyme. So negative |
feedback inhibition by product and
activity of the nerve. Constant nerve activity increases synthesis of enzymes involved in Catecholamine |
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Serotonin synthesis, tryptophan is the limiting substrate because i
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is not abundant in our diets
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is the limiting factor because is
not abundant |
on our diet. What happens when
tryptophan intake is high? An increase in insulin during a meal which activates amino acid carriers in the liver, and many of these carriers take up preferentially tyrosine and phenylalanine leading to an increase of tryptophan in our blood stream. Once the blood reaches the brain it is absorbedati by the amino carriers in the brain. So more tryptophan gets into |
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Melatonin synthesis requires
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serotonin. Light regulates its pathway by decreasing the amount of melatonin
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In nonhuman mammal in the pineal gland melatonin has
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a tropic effect negative by having less fsh and lsh when dark. When photoperiod grows longer bird testes grow 40 folds because LSH and FSH increase
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Peptide NTs are regulated at the level of
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cleavage
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On glutanergic neurons what kind of transporters present?
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excitatory AA
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GABA transaminase and glutamate decarboxylase both
have |
a pyridoxal cofactor (folate is increased when
there is a lack of this cofactor) |
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if there's hydroxine
overdose, there's convulsion because |
convulsion because the amount of
GABA is inhibited. Similarly lesser toxic amounts of hydroxine which inhibit GABA transaminase which increases GABA leading to neuropathy |
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where does Acetylcholinestarse break down acetylcholine
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extracellulary
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